牛痘疫苗接种家兔炎症皮肤提取物及连续星状神经节注药治疗头面部疱疹后神经痛临床研究

目的:三叉神经带状疱疹后神经痛是头面部疼痛疾病中最为剧烈的疼痛疾病之一。本文报道使用牛痘疫苗接种家兔炎症皮肤提取物(神经妥乐平)及连续星状神经节注药(CSGB)对比药物治疗三叉神经区疱疹后遗神经痛的临床疗效分析。方法:本组40例患者,病程3个月~4年。使用VAS评分评价疼痛程度;使用改良HAMD评价抑郁程度;同时检查治疗前、后损伤区域红外热图。门诊(OP)组治疗方法:甲钴胺2 mg/日,神经妥乐平2~4片/日,加巴喷丁600~900 mg/日或普瑞巴林150~450 mg/日。住院(IP)组治疗方法:口服药同OP组,CSGB处方:0.1%罗哌卡因200 ml+神经妥乐平6 ml,连接PCA泵(ZBB-Ⅰ型,南通产),持续量0.5~1 ml/h,追加剂量0.5 ml/次,持续使用一周。两组患者均于治疗两周及随访一年后评价效果。结果:患者主诉头面部自发性闪电样疼痛、刀割样疼痛、烧灼样疼痛为主。两组患者平均HAMD评分为21.8±3.8分,平均VAS评分为7.8±1.6分。经过治疗后OP组和IP组患者平均VAS评分分别为5.4±1.2:3.2±0.8分,HAMD评分为18.5±3.1:11.2±2.1分;复发率为45%:20%;治疗前、后局部红外热图平均差值为:1.2~5.8℃。IP组经过14~18个月的随访,疗效相对稳定。对于复发患者则采用其他方法进行治疗。结论:两组头面疱疹后神经痛患者初步结果表明:与OP组治疗结果比较,IP组加用CSGB方法安全,有效,能够快速控制剧烈疼痛,患区后遗症状大部分缓解。经过一年左右随访大部分患者效果稳定,生活质量明显改善。     

水冷射频治疗头面部带状疱疹后神经痛的护理

目的 总结水冷射频治疗头面部难治性带状疱疹后神经痛的围手术期护理方法.方法 对13例患者进行回顾性分析.结果 患者术后疼痛视觉模拟评分(VAS)明显低于术前(P＜0.01),术后并发的严重水肿在2～3周内明显减轻或消退.结论 水冷射频治疗头面部难治性带状疱疹后神经痛疗效确切,围术期护理方法安全、可行,值得推广.     

水冷射频治疗头面部难治性带状疱疹后神经痛

目的:评估水冷射频治疗头面部难治性带状疱疹后神经痛的临床可行性.方法:对11例头面部难治性带状疱疹后神经痛、经传统射频治疗后效果欠佳患者行水冷射频治疗,记录治疗前及治疗后1天、7天、14天、1个月和6个月时疼痛数字评分(NRS)及并发症发生情况.结果:患者治疗后NRS显著下降(P＜0.01),术后出现治疗局部软组织肿胀,1～2周内缓解.结论:水冷射频治疗头面部难治性带状疱疹后神经痛效果确切、安全.     

CT引导下单次脉冲射频治疗头面部带状疱疹后神经痛的疗效分析

目的:观察和分析CT引导下选择性三叉神经单次脉冲射频治疗头面部带状疱疹后神经痛(pos-therpetic neuralgia, PHN)的临床效果。方法:36例头面部PHN住院病人随机分为2组:神经阻滞治疗组(A组);脉冲射频治疗组(B组)。A组在给予加巴喷丁治疗的基础上,根据受累三叉神经分支相应实施眶上、上颌、下颌神经及局部痛域皮下阻滞治疗;B组在给予加巴喷丁治疗的基础上,根据受累三叉神经分支相应实施CT引导下眶上神经、上颌神经和下颌神经脉冲射频治疗。治疗前及疗程完成后第3天、3月和12月进行疼痛程度评估。结果:各组疗程完成后第3天视觉模拟评分法(visual analogue scale, VAS)评分均较治疗前减低(P <0.05)。疗程完成后3月和12月各组治疗显效率均达60%以上,A组和B组显效率比较无统计学差异(P> 0.05)。各例治疗过程中均无严重并发症发生。结论:CT引导下选择性三叉神经单次脉冲射频是治疗头面部PHN安全而有效的方法,但临床效果不优于神经阻滞治疗。     

三叉神经半月节阻滞与三叉神经干阻滞治疗急性带状疱疹性三叉神经痛的疗效对比

三叉神经是带状疱疹常见的受累部位,多数患者伴有头面部剧烈疼痛,严重影响患者的正常生活,并可延续成为疱疹后神经痛.为了最大限度地消除疼痛、减少带状疱疹后神经痛的发生,临床上及早控制疼痛尤为重要.我们对有重度疼痛的急性带状疱疹性三叉神经痛患者,进行了三叉神经半月节和三叉神经干阻滞的疗效对比,现报道如下.     

头面部带状疱疹65例临床分析

目的:通过对65例头面部带状疱疹患者的临床分析,以探讨头面部带状疱疹患者的临床表现、治疗和预后的特点。方法:分析65例头面部带状疱疹患者的临床情况。结果:65例患者,平均发病年龄45.1岁。好发于春秋季(66%),大部分有明确诱发因素。皮损分布多在三叉神经(63%)。寻常性皮损占89%。并发症有疱疹后遗神经痛占38%。结论:头面部带状疱疹病情重,并发症多。治疗该病的关键是抗病毒治疗及联合应用小剂量糖皮质激素,对减轻神经痛十分有效。     

带状疱疹后神经痛临床调查分析

目的:带状疱疹后神经痛是周围神经受到病毒损伤后的疼痛疾病中最有代表性的疾病之一,本文报道疼痛科集中6年来调查、统计的临床病例结果.方法:2004年起使用神经痛表共统计门诊、住院及会诊的带状疱疹后神经痛患686例,主要观察疼痛程度和性质、临床类型、患区遗留症状和伴随症状.结果:患者主诉以自发性闪电样疼痛、刀割样疼痛、烧灼样疼痛、针刺样疼痛和混合性疼痛为多见.平均VAS评分为6.8分.患者临床表现为4种类型的变化,分别为激惹型(57.14%)、麻痹型(22.16%)、整合型(17.93%)和无激惹型(2.77%).结论:本组疱疹后神经痛患者调查表明:大部分患者疼痛时间均超过3-6个月,最长达8年.疼痛程度为中、重度.患者的生活质量、工作能力均明显受影响.     

脉冲射频治疗三叉神经带状疱疹后神经痛的疗效观察

带状疱疹后遗神经痛(postherpetic neuralgia, PHN)表现为持续性疼痛(几个月甚至几年),临床上一般疱疹消失后,相应的感觉神经支配区仍然遗留或重新出现疼痛.三叉神经区疱疹后遗神经痛由于解剖位置特殊加上发病初期治疗的不到位或不规范,可遗留顽固性疼痛.PHN保守治疗疗效差,而手术治疗风险大,患者不愿意接受.本科用脉冲射频治疗三叉神经PHN,取得了良好的临床效果.     

脉冲射频V_1与C_(2-3)后内侧支治疗额面部带状疱疹后神经痛

目的:评价第五对脑神经即三叉神经第一支(V1)联合颈2-3(C2-3)后内侧支脉冲射频治疗额面部带状疱疹后神经痛的疗效。方法:30名额面部带状疱疹后神经痛患者随机分为V1脉冲射频组(V组,n=15)和C2-3后内侧支联合V1脉冲射频组(C组,n=15)。比较两组治疗前、治疗后第1、7、14天、1、3、6个月的视觉模拟评分(visual analogue scale,VAS)及治疗的副作用;比较两组治疗前及治疗后第1、7、14天及1个月的曲马多日用量;比较两组治疗前、治疗后第1、3、6个月的匹兹堡睡眠质量指数(pittsburgh sleep quality index,PSQI)。结果:与治疗前比较,两组患者治疗后VAS值、曲马多日用量及PSQI评分均显著下降(P<0.05)。治疗后第1天,C组VAS值及曲马多日用量均明显低于V组(P<0.05);但随后各时点两组VAS值、曲马多日用量及PSQI评分差异均无统计学意义。两组患者均无明显不良反应。结论:对于额面部带状疱疹后神经痛患者,联合C2-3后内侧支脉冲射频可增强即时V1的射频镇痛效果,但远期疗效无区别。     

经皮穿刺圆孔射频治疗上颌神经痛的临床研究

目的:探讨经皮穿剌圆孔射频治疗上颌神经痛的疗效。方法:对21例内科治疗失败或有创治疗后复发的上颌神经痛患者,在X线引导下,将头端塑形的普通射频穿刺针,以前下方入路经皮经翼腭窝穿刺圆孔,对上颌神经干行射频温控热凝处理。以视觉模拟评分法(visual analoguescale,VAS)记录患者术前、术后72小时以及术后随访期内疼痛程度来评价治疗疗效。结果:对21患者成功施行23次上颌神经干射频热凝术。21例患者术前VAS评分7.4±1.6分。术后72小时所有患者VAS评分均为0分。手术后随访时间4周到9周(平均31周),未出现上颌神经痛复发。术后上颌神经分布区面部麻木感发生率95.2%(20/21),面部肿胀发生率38.1%(8/21),无角膜感觉神经功能损伤病例发生。结论:经皮穿刺圆孔射频温控热凝处理上颌神经干治疗三叉神经上颌支痛是安全和有效的。     

Herpes zoster and post-herpetic neuralgia

Pain associated with herpes zoster arise from the virul neuritis of the suffered trigeminal or spinal dorsal ganglion. Prolonged neuritis makes an irreversible nerve injury and continuous pain impulse develops a central sensitization. A post-herpetic neuralgia is thought to be a neuropathic pain due to the irreversible nerve injury and sensitization. It is important to treat herpetic pain completely before the development of the post-herpetic neuralgia, because there are few effective therapies to cure post-herpetic neuralgia. A sympathetic nerve block increases the nerve blood flow supply, and may improve the nerve injury. It is also known that some sympathetic mechanisms relate to the development of the sensitization. A sensory nerve block reduces pain impulse to the dorsal horn, and may interfere the sensitization. A cortico-steroid administrated with a nerve block can reduce the neuritis, and may improve the nerve injury.     

Topical lidocaine reduces pain in post-herpetic neuralgia

We report the results of a single session, non-blinded, trial of topical application of 10% lidocaine in gel form to the painful skin of 11 patients with well established post-herpetic neuralgia (PHN). Pain decreased as measured by 100 mm VAS pain scale and 100 mm VAS pain relief scale in both trigeminal and thoracic PHN patients.     

Post-herpetic neuralgia: further post-mortem studies of cases with and without pain.

The pathological features associated with post-herpetic neuralgia require further study. We report here 5 cases, 3 with severe post-herpetic neuralgia (PHN) and 2 with no persistent pain. The findings of dorsal horn atrophy and cell, axon and myelin loss with fibrosis in the sensory ganglion were found only in patients with persistent pain. Marked loss of myelin and axons in the nerve and/or sensory root were found in cases with and without pain. Some evidence is presented for a more generalized subacute or chronic inflammatory process which may explain the clinical features of some patients. Further studies will be necessary to fully describe the morbid anatomy of this disorder.     

Diagnosis and differential diagnosis of trigeminal neuralgia.

Trigeminal neuralgia is a chronic facial pain classified as a neuropathic pain. There is widespread agreement regarding the International Association for the Study of Pain definition of classical idiopathic trigeminal neuralgia as "a sudden, usually unilateral, severe, brief, stabbing, recurrent pain in the distribution of one or more branches of the fifth cranial nerve." However, there are variations in presentation that are less easy to diagnose and an erroneous diagnosis of trigeminal neuralgia is occasionally made. In patients with tumors or multiple sclerosis, trigeminal neuralgia is termed secondary. Currently, clinical manifestations are the mainstay for diagnosis because there are no objective tests to validate the diagnosis. The sensitivity and specificity of these clinical manifestations is reviewed. Magnetic resonance imaging (MRI) and three-dimensional fast-in-flow with steady-state precession MRI are performed to determine the presence of tumors or plaques of multiple sclerosis and to assess possible compressions and deformations of the trigeminal nerve. Their specificity and sensitivity regarding compressions found at the time of surgery is reviewed. Other differential diagnoses for chronic unilateral orofacial pain are discussed.     

Studies on the operative outcomes and mechanisms of microvascular decompression in treating typical and atypical trigeminal neuralgia

OBJECTIVE: To evaluate the operative outcomes and mechanisms of microvascular decompression in treating typical and atypical trigeminal neuralgia. METHODS: A group of 45 patients with typical trigeminal neuralgia and 17 patients with atypical trigeminal neuralgia treated by micro-vascular decompression from 2000 to 2002 were reviewed, including their clinical presentations, operative findings, and outcomes. RESULTS: Of 45 patients with typical trigeminal neuralgia, the mean duration was 3.1 years, and the mean age of pain onset was 60.3 years. Single trigeminal division was involved in 20 patients (44.4%), and 2 or 3 divisions were involved in the other 25 patients (55.6%). During the operation, artery compression was found in 39 patients (86.7%), and the combined artery and venous compression was found in 6 patients (13.3%). Postoperatively, complete pain relief was achieved in 44 patients (97.8%), and significant pain relief was achieved in 1 patient (2.2%). As for 17 patients with atypical trigeminal neuralgia, the mean duration and the mean age of pain onset was 8.7 years and 55.5 years, respectively. Two or 3 trigeminal divisions were involved in all of these patients. During operation, artery compression occurred in 10 patients (58.8%), and the combined artery and venous compression was found in 7 patients (41.2%). Postoperatively, complete pain relief was achieved in 5 patients (29.4%), and partial pain relief was achieved in 10 patients (58.8%), and 2 patients showed no response to microvascular decompression. CONCLUSIONS: The operative outcome of microvascular decompression in patients with typical trigeminal neuralgia was better than that of patients with atypical trigeminal neuralgia, which perhaps related to short duration, late onset of pain, limited distribution, artery compression, and complete operative decompression.     

Antiepileptic drugs in the management of cluster headache and trigeminal neuralgia

Cluster headache and trigeminal neuralgia are relatively rare but debilitating neurologic conditions. Although they are clinically and diagnostically distinct from migraine, many of the same pharmacologic agents are used in their management. For many patients, the attacks are so frequent and severe that abortive therapy is often ineffective; therefore, chronic preventive therapy is necessary for adequate pain control. Cluster headache and trigeminal neuralgia have several distinguishing clinical features. Cluster headache is predominantly a male disorder; trigeminal neuralgia is more prevalent in women. Individuals with cluster headaches often develop their first attack before age 25; most patients with trigeminal neuralgia are between age 50 and 70. Cluster headaches are strongly associated with tobacco smoking and triggered by alcohol consumption; trigeminal neuralgia can be triggered by such stimuli as shaving and toothbrushing. Although the pain in both disorders is excruciating, cluster headache pain is episodic and unilateral, typically surrounds the eye, and lasts 15 to 180 minutes; the pain of trigeminal neuralgia lasts just seconds and is usually limited to the tissues overlying the maxillary and mandibular divisions of the trigeminal nerve. Cluster headache is unique because of its associated autonomic symptoms. Although the pathophysiology of cluster headache and trigeminal neuralgia are not completely understood, both appear to have central primary processes, and these findings have prompted investigations of the effectiveness of the newer antiepileptic drugs for cluster headache prevention and for the treatment of trigeminal neuralgia. The traditional antiepileptic drugs phenytoin and carbamazepine have been used for the treatment of trigeminal neuralgia for a number of years, and while they are effective, they can sometimes cause central nervous system effects such as drowsiness, ataxia, somnolence, and diplopia. Reports of studies in small numbers of patients or individual case studies indicate that the newer antiepileptic drugs are effective in providing pain relief for trigeminal neuralgia and cluster headache sufferers, with fewer central nervous system side effects. Divalproex has been shown to provide effective pain control and to reduce cluster headache frequency by more than half in episodic and chronic cluster headache sufferers. Topiramate demonstrated efficacy in a study of 15 patients, with a mean time to induction of cluster headache remission of 1.4 weeks (range, 1 day to 3 weeks). In the treatment of trigeminal neuralgia, gabapentin has been shown to be effective in an open-label study. When added to an existing but ineffective regimen of carbamazepine or phenytoin, lamotrigine provided improved pain relief; it also may work as monotherapy. Topiramate provided a sustained analgesic effect when administered to patients with trigeminal neuralgia. The newer antiepileptic drugs show considerable promise in the management of cluster headache and trigeminal neuralgia.     

Iontophoresis of vincristine versus saline in post-herpetic neuralgia. A controlled trial

Twenty patients with post-herpetic neuralgia (median duration 28.5 months) were randomly allocated to receive transdermal iontophoresis of either vincristine or saline. Although significant improvement in pain by word score and visual analogue scale (P = 0.05) was reported by 6 out of 10 of the vincristine group, none of the patients considered themselves 'cured.' There was no significant change in the saline group. No adverse haematological or neurological side effects were seen, but skin irritation and painless electrical burns were common in both groups. The dramatic relief of pain in patients with post-herpetic neuralgia of 3 months or less reported elsewhere was not seen in our group who had pain of a longer duration. This present trial does not confirm the value of vincristine iontophoresis in the treatment of post-herpetic neuralgia of over 6 months duration.     

A型肉毒毒素治疗三叉神经痛和带状疱疹后神经痛的临床疗效

目的：观察A型肉毒毒素治疗三叉神经痛和带状疱疹后神经痛的临床效果。方法：选取33例三叉神经痛或带状疱疹后神经痛患者，进行疼痛区域A型肉毒毒素皮下或皮内注射治疗，评估患者治疗时、治疗2周后、治疗3个月后疼痛情况（NRS）、睡眠状况及生活质量（QOL），判断治疗效果，观察药物不良反应。结果：患者使用A型肉毒毒素治疗2周后、3个月后疼痛评分、睡眠评分显著低于治疗时（P<0.05），生活质量显著高于治疗时（P<0.05），治疗效果好，不良反应少。结论：A型肉毒毒素治疗三叉神经痛和带状疱疹后神经痛效果显著，可成为神经病理性疼痛治疗的一种新途径。     

Facial pain and the second edition of the International Classification of Headache Disorders

BACKGROUND: Recurrent or chronic facial pain may be a diagnostic challenge. Applying the diagnostic criteria of the second edition of the International Classification of Headache Disorders (ICHD-II) leaves a considerable number of patients unclassifiable. OBJECTIVE: The aim of this study was to establish and evaluate revised criteria of trigeminal neuralgia and persistent idiopathic facial pain. METHODS: Based on the diagnostic value of 12 clinical features of trigeminal neuralgia and 15 features of persistent idiopathic facial in 97 patients referred for facial pain to a neurological tertiary care centre we established revised criteria for persistent idiopathic facial pain and additional criteria for probable trigeminal neuralgia and probable idiopathic facial pain. RESULTS: Applying the newly proposed criteria reduced the number of patients with facial pain not classifiable by more than 50%. The new criteria improved the sensitivity, particularly in idiopathic facial pain and did not cause a relevant decrease in specificity compared to ICHD-II. CONCLUSION: This study suggests that amendments to the ICHD-II criteria improve the diagnostic classification of facial pain.